Inflammatory Bowel Disease (IBD) and Osteoporosis

Osteoporosis is a decrease in bone density. As humans age, resorption of bone outpaces formation of bone and bone density begins to decline. While some loss of bone density is normal, when the process accelerates, osteoporosis becomes a threat. While some people with osteoporosis may notice some back pain or change in posture, this disorder generally produces no symptoms until the bone becomes so weakened that it breaks. Bone fractures due to osteoporosis most often occur in the spine and hips. For this reason, it is very important to screen for bone loss with bone density testing, and to take preventive measures to halt bone loss.

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Osteoporosis is more common in patients with inflammatory bowel disease than the general population. It is more common in Crohn's patients than Ulcerative Colitis, occurring in up to 30% of Crohn's patients. Patients with inflammatory bowel disease therefore develop osteoporosis at younger ages than the general population. Additionally, while rare in men, osteoporosis is not uncommon in men with inflammatory bowel disease. There are many reasons for bone loss to develop in patients with inflammatory bowel disease.

Patients with inflammatory bowel disease have elevated levels of specialized proteins, which increase the body's inflammatory response. These proteins may disrupt normal bone metabolism, leading to more rapid resorption of bone compared to formation. Additionally, patients with more active forms of Crohn's are at increased risk of developing osteoporosis because they have greater concentrations of such proteins. These proteins, cytokines, are less common in ulcerative colitis, and likely in part explain the decrease incidence of osteoporosis in Ulcerative colitis compared with Crohn's disease.

Another reason for the increased incidence of osteoporosis in inflammatory bowel disease is vitamin D deficiency. Vitamin D is required for the absorption of calcium.

As vitamin D is absorbed in the small intestine, patients with Crohn's disease, especially those who have undergone small bowel resection or who have extensive small bowel involvement, are at increased risk for vitamin D deficiency. Vitamin D deficiency results in reduced calcium absorption and leads to poor bone mineralization and an increased incidence of osteoporosis.

A final factor that leads to the development of osteoporosis in patients with inflammatory bowel disease is the use of corticosteroids. Almost 50% of patients who take corticosteroids on a long-term basis develop osteoporosis, with the odds correlating with the dose and length of time that a person is on them. Steroids work to impair the formation of new bone by decreasing the amount of calcium absorbed by the intestines from food, increasing the excretion of calcium in the urine, stimulating the production of cells that break down bone, decreasing the number of bone-forming cells and reducing the production of the hormone estrogen, which contributes to strong bones. It is felt that steroid use plays a large role in the development of osteoporosis in patients with Ulcerative colitis.

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Patients with inflammatory bowel disease therefore need to be screened more frequently for osteoporosis than the general population. Every effort should be made to use steroid-sparing medications to treat inflammatory bowel disease, such as immunosuppressives (6-MP and Imuran) and safer steroids such as Entocort. Medications that enhance bone growth, such as Fosamax and Actonel should be started earlier than in the general population. Additionally, patients with inflammatory bowel disease, especially with evidence of osteoporosis should try to restrict alcohol consumption, stop smoking, engage in regular physical activity, eat a diet rich in calcium and vitamin D.